Myocardial infarction is the greatest killer of mankind. The greatest hazards to the victim occur in the early stages of infarction and in the immediate post-infarct period. We know relatively little of the fundamental and dynamic patho-physiologic alterations which occur during cardiac injury and repair. The May Institute has developed an experimental model for the study of myocardial infarction. The potent beta-adrenergic stimulating agent, isoproterenol, is used to induce severe myocardial infarction by causing such intense, increased cardiac output that a state of coronary insufficiency is created followed by anoxia and necrosis. The changes in the myocardium, in serum enzymes, lipids, etc. resemble the myocardial infarct syndrome as it occurs in man. This experimental facsimile of human myocardial infarction is being investigated to determine how certain physiological and pathological events may be inter- related, i.e., myocardial connective tissue, enzyme lipid, catecholamine and adrenal steroid changes. More specifically, biochemical investigations - correlated with histologic and histochemical studies - will be made of the dynamic changes in ground substance, e.g., mucopolysaccharides, and connective tissue elements, e.g., collagen, which occur during the crucial stages of myocardial necrosis and repair, e.g., scar tissue formation. When sufficient insight is obtained concerning the basic processes of myocardial damage and repair, investigations will be extended to determine how various conditions, e.g., exercise, drugs, etc. will benefit or adversely affect the myocardial repair process with applicability toward development of therapeutic measures which would insure or hasten cardiac repair.